1. G cells in antrum of stomach or duodenum
2. G17 dominant in gastric G cells, G17/G34 mixed in duodenum
3. Stimulates histamine release from ECL cells in body of stomach
4. Gastric acid induces the release of somatostatin from antral D cells, which inhibits histamine release and parietal cell activity

1. Duodenal I cells
2. Meals rich with protein and fat
3. CCK potentiates secretin-induced bicarbonate exposure, inhibits gastric empyting (directly on pylorus and indirectly on vagus nerve), inhibits gastric acid secretion (acts on somatostatin secreting D cells)

Vagal control

Verner-Morrison syndrome

Watery diarrhea-achlorhydria-hypokalemia

Generally inhibitory (gastric acid secretion, motility, secretion of insulin/glucagon/PP, splachnic gut flow)

Note: short half-life. Synthetic analogue (octreotide) is used to treat neuroendocrine tumors, secretory diarrheas, and acromegaly

PP (endocrine cells), PYY (neuron/endocrine cells), NPY (neural cells)

PP produced in PP islet. Induced by meal intake (vagal phase, gastric distension/gastric phase, and intestinal phase/presence of nutrients). Believed to suppress appetite.

Plasma levels increased in gastrointestinal endocrine tumors

Released in response to meal; ""ileal brake"

Enhanced in patients with malabsorption in order to delay gastic empyting and increase digest absportive efficiency

1. Ascites
2. Functional renal failure
3. Sodium and water retention
4. Collateral circulation
5. Hypersplenism
6. Hepatopulmonary syndrome
7. Cardiomyopathy

1. Deficiency in clotting factors
2. Hypoproteinemia
3. Impaired metabolic functions
4. Hepatic encephalopathy

No basement membrane, fenestrae, produce NO (acts as vasodilator)

Lack of NO production increases vasoconstriction. Capillarization removes fenestration. Space of Disse widened by collagen deposition, preventing communication.

1. Hyperdynamic circulation
2. Systemic vasodilatation (and consequent noradrenaline secretion)
3. Sodium avidity

Increase of lymph fluid due to sinusoidal occlusion

Increase in intrahepatic pressure interferes with drainage of fluid from intestines, which escape into abdominal cavity due to increased membrane permeability

Type 1: Progressive impairment, doubling of baseline serum creatine to above 2.5 mh/dl in less than two week

Type 2: Slow, progressive impairment

1. Low clearance (<40mL/min, serum creatinine >1.5 mg/dl) due to renal hypoperfusion
2. Oliguria
3. Low urine sodium concentration (<10 mEq/L)
4. Normal renal sonogram, no proteinuria or hematuria; unaffected by diuretics or volume expansion

No; while ammonia has been shown to inhibit GABA sequestration by astrocytes (leading to increased GABA-inhibition), an increase in BZ (benzodiazepines) is also hypothesized to be necessary. BZ poteniate GABA receptors.

Additionally, neurosteroid production is believed to be upregulated by ammonia via increase in BZ receptors and stimulation of astrocyte mitochondria

Increased peripheral, decreased hepatic NO production.

Increase in peripheral from endothelial cells, decrease in liver is from damage to sinusoidal cells.

1. Portosystemic shunting
2. Impaired RE cells
3. Intestinal bacterial relocate to lymph
4. Increased intestinal permeability
5. Contamination of ascites fluid (spontaneous bacterial peritonitis)
6. Bleeding

1. Reye syndrome (young child given aspirin for acute viral infection)
2. Fatty liver of pregnancy
3. Tetracycline toxicity

1. Centrilobular pattern of injury due to increased NADH levels and increased acetylaldehyde production
2. Hepatocellular necrosis with polymorphonuclear cell infiltration and alcholic cell hyalin deposition (Mallory bodies)
3. Pericentral fibrosis

Identify:

[image]

What is the most lkely etiology?

Macronodular cirrhosis. Most likely sequela of chronic active hepatitis. Can also be caused by progression of micronodular alcholic cirrhosis. Note irregularity distinguishes it from micronodular.

Most likely cirrhosis to lead to hepatocarcinoma.

1. Budd-Chiari syndrome - oral contraceptives
2. Veno-occlusive disease - antimetabolites
3. Peliosis hepatitis - androgenic steroids
4. Angiosarcome - vinylchloride monomer

Metabolization by cytochrome P-450 leads to toxic intermediates.

Alchohol exacerbates toxicity by increasing P-450 and decreasing available GSH

Treatment = N-acetylcystein, acute toxic dose > 10 g, chronic toxic dose > 3 g/day

1. Disregulation of cytotoxic T cells, impaired regulatory CD4+25+ T cells
2. Type 1 = lupoid features (HLA-DRB1 and HLA-DQB1) with antibodies against actin and pANCA; Type 2 = anti-LKM, Mediterranean children
3. Similar to chronic hepatitis

Biopsy, followed by silver staining (to observe curved, rod-shaped organism) and H&E for inflammatory exudate

Nondefinitive test is urea breath test measures CO2 evolved from breakdown of urea. H. pylori is difficult to culture.

1. Hydrogen breath test
2. Radioactive bile salts
3. Radioactive chromium-albumin
4. D-xylose absorption test

Trypsinogen --> Trypsin

Activation of digestive enzymes --> necrosis

Microvascular leakage --> edema --> necrosis of fates --> inflammatory reaction --> proteolytic destruction of tissue --> hemorrhage

Neutral fats break down, fatty aaids combine with calcium to form soaps

Hypocalcemia, jaundice (biliary obstruction), sepsis-like syndrome, systemic immune response

Serum amylase, serum lipase (elevated for 8-14 days, sensitive and specific), serum trypsinogen rises rapidly 10-20x (frequent false positives, but sensitive)

Risk factors: smoking, black and Native American, 60+ y/o, chronic pancreatitis + DM

60% arise in head, 10% in body, 10% tail, 20% diffuse

Biliary duct obstruction in head, with painless dilatation of gallbladder (Courvoisier sign). Migratory thrombophlebitis (Trousseau sign) in 10% ESPECIALLY IN TAIL

1. Accumulation of pigment material in tissue sections
2. Ballooned hepatocytes with wispy cytoplasm
3. Dilated canaliculi around terminal hepatic vein

1. Portal tract edema and periductular inflammation (neutrophils)
2. Proliferation of bile ductular structures
3. Superimposed bacterial infection in biliary tree (neutrophils)

Cholesterol supersaturation, GB hypomotility and GB mucin gell accumulation

Supersaturation due to genetic and environmental factors

Hypomotility due to CKK

Mucin accumulation from hypersecretion (unknown stimulus)